Asymmetric dimethylarginine
(Synonyms: N5-[(二甲基氨基)亚氨基甲基]-L-鸟氨酸) 目录号 : GC32457
An endogenous NOS inhibitor
Cas No.:30315-93-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
NG,NG-dimethyl-L-arginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS).1,2 It is formed from arginine by protein arginine methyltransferases (PRMTs) and degraded by dimethylarginine dimethylaminohydrolases (DDAHs) and alanine-glyoxylate aminotransferase 2 (AGXT2).1 ADMA levels are increased concomitant with an increase in blood pressure in Dahl salt-sensitive rats fed a high-salt diet.2 ADMA levels are increased in the plasma in a variety of endothelial dysfunction-related diseases, including hypertension, congestive heart failure, and end-stage renal disease.1,3,4
1.Sydow, K., and Münzel, T.ADMA and oxidative stressAtheroscler. Suppl.4(4)41-51(2003) 2.Jin, J.S., and D'Alecy, L.G.Central and peripheral effects of asymmetric dimethylarginine, an endogenous nitric oxide synthetase inhibitorJ. Cardiovasc. Pharmacol.28(3)439-446(1996) 3.Vallance, P., Leone, A., Calver, A., et al.Accumulation of an endogenous inhibitor of nitric oxide synthesis in chronic renal failureLancet339(8793)572-575(1992) 4.Matsuoka, H., Itoh, S., Kimoto, M., et al.Asymmetrical dimethylarginine, an endogenous nitric oxide synthase inhibitor, in experimental hypertensionHypertension29(1 Pt 2)242-247(1997)
| Cas No. | 30315-93-6 | SDF | |
| 别名 | N5-[(二甲基氨基)亚氨基甲基]-L-鸟氨酸 | ||
| Canonical SMILES | CN(C)C(NCCC[C@H](N)C(O)=O)=N | ||
| 分子式 | C8H18N4O2 | 分子量 | 202.25 |
| 溶解度 | Water : 150 mg/mL (741.66 mM);Water : 100 mg/mL (494.44 mM) | 储存条件 | Store at -20°C, stored under nitrogen |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.9444 mL | 24.7219 mL | 49.4438 mL |
| 5 mM | 0.9889 mL | 4.9444 mL | 9.8888 mL |
| 10 mM | 0.4944 mL | 2.4722 mL | 4.9444 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Asymmetric dimethylarginine: An crucial regulator in tissue fibrosis
Eur J Pharmacol 2019 Jul 5;854:54-61.PMID:30951718DOI:10.1016/j.ejphar.2019.03.055.
Fibrosis is a reparative process with very few therapeutic options to prevent its progression to organ dysfunction. Chronic fibrotic diseases contribute to an estimated 45% of all death in the industrialized world. Asymmetric dimethylarginine (ADMA), an endothelial nitric oxide synthase inhibitor, plays a crucial role in the pathogenesis of various cardiovascular diseases associated with endothelial dysfunction. Recent reports have focused on ADMA in the pathogenesis of tissue fibrosis. This review discusses the current knowledge about ADMA biology, its association with risk factors of established fibrotic diseases and the potential pathophysiological mechanisms implicating ADMA in the process of tissue fibrosis.
Asymmetric dimethylarginine and angiogenesis: biological significance
Int Angiol 2018 Dec;37(6):431-436.PMID:30256050DOI:10.23736/S0392-9590.18.04017-8.
Competitive inhibition of endothelial nitric oxide synthase (eNOS) is the main biological effect of Asymmetric dimethylarginine (ADMA), i.e. the methylated derivative of L-arginine. The resulting low level of NO is becoming one of the elements of pathogenesis of numerous cardiovascular disorders, mainly related to atherosclerosis, but also other metabolic diseases including type 2 diabetes. It appears that a high level of ADMA is not only a marker of pathological conditions such as chronic kidney failure, but also a significant factor which damages the endothelium. Despite multiple studies, the mechanisms of reducing the level of ADMA, which would allow to inhibit the progression of cardiovascular diseases and effective treatment, e.g. by means of L-arginine supplementation or medicines which are lowering ADMA levels, are still unclear. Perhaps, linking ADMA with the processes of new blood cell formation (angiogenesis) will allow us to explain these multifactor mechanisms.
Asymmetric dimethylarginine: a Key Player in the Pathophysiology of Endothelial Dysfunction, Vascular Inflammation and Atherosclerosis in Rheumatoid Arthritis?
Curr Pharm Des 2021;27(18):2131-2140.PMID:33413061DOI:10.2174/1381612827666210106144247.
Patients with rheumatoid arthritis (RA), a chronic and disabling autoimmune condition that is characterized by articular and extra-articular manifestations and a pro-inflammatory and pro-oxidant state, suffer from premature atherosclerosis and excessive cardiovascular disease burden. A key step in the pathogenesis of atherosclerosis is impaired synthesis of the endogenous messenger nitric oxide (NO) by endothelial cells which, in turn, alters local homeostatic mechanisms and favors vascular damage and plaque deposition. While the exact mechanisms of endothelial dysfunction in RA remain to be established, there is good evidence that RA patients have relatively high circulating concentrations of the methylated arginine Asymmetric dimethylarginine (ADMA), a potent endogenous inhibitor of endothelial NO synthase (eNOS). This review discusses the biological and pathophysiological role of ADMA, the interplay between ADMA, inflammation and oxidative stress, and the available evidence on the adverse impact of ADMA on endothelial function and atherosclerosis and potential ADMA-lowering therapies in RA patients.
Asymmetric dimethylarginine in psychiatric disorders
Psychiatry Res 2021 Jun;300:113901.PMID:33819866DOI:10.1016/j.psychres.2021.113901.
Serum concentrations of Asymmetric dimethylarginine (ADMA) in patients with schizophrenia, schizoaffective disorder, bipolar disorder, and depression were determined and compared to serum concentrations in healthy individuals. In all psychiatric diseases investigated, the ADMA concentration was elevated compared to the control group. Patients with recurrent depressive disorder had higher ADMA levels than patients with only one depressive episode. No differences between women and men were found. The elevated ADMA levels suggest that ADMA is involved in the pathophysiology of psychiatric diseases.
Toxic Dimethylarginines: Asymmetric dimethylarginine (ADMA) and Symmetric Dimethylarginine (SDMA)
Toxins (Basel) 2017 Mar 6;9(3):92.PMID:28272322DOI:10.3390/toxins9030092.
Asymmetric and symmetric dimethylarginine (ADMA and SDMA, respectively) are toxic, non-proteinogenic amino acids formed by post-translational modification and are uremic toxins that inhibit nitric oxide (NO) production and play multifunctional roles in many human diseases. Both ADMA and SDMA have emerged as strong predictors of cardiovascular events and death in a range of illnesses. Major progress has been made in research on ADMA-lowering therapies in animal studies; however, further studies are required to fill the translational gap between animal models and clinical trials in order to treat human diseases related to elevated ADMA/SDMA levels. Here, we review the reported impacts of ADMA and SDMA on human health and disease, focusing on the synthesis and metabolism of ADMA and SDMA; the pathophysiological roles of these dimethylarginines; clinical conditions and animal models associated with elevated ADMA and SDMA levels; and potential therapies against ADMA and SDMA. There is currently no specific pharmacological therapy for lowering the levels and counteracting the deleterious effects of ADMA and SDMA. A better understanding of the mechanisms underlying the impact of ADMA and SDMA on a wide range of human diseases is essential to the development of specific therapies against diseases related to ADMA and SDMA.